LAB DIAGNOSIS AND

MANAGEMENT OF COMA

(UNCONCIOUS PATIENT)

Professor Dr. Abdus Salam KhanProfessor Dr. Abdus Salam KhanMBBS, M.Phil, PhD

HOD Pathology

Women Medical College Abbottabad

Definition

Persistent loss of consciousness

or coma is a state in which patient is

totally unaware of both self and

external surroundings and unable to

respond meaningfully to external respond meaningfully to external

stimuli

The Unconscious Patient

Challenges in assessment

Multiple and varied causes of coma

Limited time availability for diagnosis & therapeutic judgementjudgement

Adopt precise clinical and investigatory approach

Supportive laboratory tests give indirect information

and require time

Duty of a physicianTo arrive at a diagnosis

To predict the prognosis as there is nothing more

wasteful than exhausting resources in treating patients

who will remain in a “persistent vegetative state” who will remain in a “persistent vegetative state”

Metabolic

drugsdrugs

hypoglycaemiahypoglycaemia

NeurologicalNeurological

vascularvascular

raised intraraised intra--cranial cranial

Recognise the principle subRecognise the principle sub--causescauses

hypoglycaemiahypoglycaemia

hypoxiahypoxia

trauma trauma

infectioninfection

raised intraraised intra--cranial cranial

pressure/reduced pressure/reduced

cerebral blood flowcerebral blood flow

epilepsyepilepsy

Clinico-pathological approach

Common causes of coma

A) Localized mass lesions producing pressure effect

i. Extradural hematomai. Extradural hematoma

ii. Acute subdural hematoma

iii. Chronic subdural hematoma

iv. Cerebral contusion

v. Brain tumor

B) Diffuse neuronal lesionsi. Infections; Meningitis

Encephalitis

Cerebral abscess

Sepsis

Cerebral malaria

ii. Metabolic encephalopathies; Diabetes mellitis

Hypoglycemia

Ketoacidosis

Hyperosmolar coma

iii. Uremia

iv. Hepatic failure; Viruses A, B, D & E, iv. Hepatic failure; Viruses A, B, D & E,

Falciparum malaria

Typhoid

Paracetamol, isoniazid

v. Myxoedema

vi. Drug overdose

vii. Haemorrhage (subarachnoid)

viii. Trauma (generalized brain oedema)

xi. Ischemia (anoxia)

x. Respiratory failure

xi. Alcohol abuse

xii. Others (Epilepsy, thiamine deficiency, psychiatric diseases)

T - trauma

I - infection

N - neoplasia

D - doctors/drugs

E - endocrine

-head injury, hypovolaemia

-sepsis, meningitis

-SOL, metabolic complications

-anaesthesia, “recreational”

-hypoglycaemia, Addison’s

The unconscious patientThe unconscious patient--surgical sievesurgical sieve

E - endocrine

A - autoimmune

D - degenerative

M - metabolic

I - idiopathic

C - congenital

E - endothelial /vascular

-hypoglycaemia, Addison’s

-K+, Na2+, Ca2+, glu, O2/CO2

-epilepsy

-CVAs/TIAs/intracerebral bleeds

Clinical evaluation of the unconscious patient

History (from relatives, friends or witnessesi. Onset of coma (abrupt, gradual)

ii. Recent complaints (headache, depression, focal weakness, vertigo)

iii. Previous medical illness (diabetes, uremia, heart disease)

iv. Access to drugs (sedatives, psychotropic drugs)

General physical examinationi. Vital signs

ii. Evidence of traumaii. Evidence of trauma

iii. Evidence of acute or chronic illness

iv. Evidence of drug ingestion (needle marks, alcohol breath)

v. Nuchal rigidity (examine with care)

Neurological examination with particular attention toi. State of conciousness

ii. Respiratory pattern

iii. Pupillary size and pattern

iv. Eye movements

v. Motor responses

Investigations

The investigatory scheme involves Imaging studies and

laboratory evaluation. Choice of diagnostic investigation

depends on suspected diagnosis.

Localized mass lesions & some diffuse brain

lesionsSkull X-raySkull X-ray

CT scan

Carotid angiography

EEG

Vertebral angiography

Ventriculography

Extradural hematoma

Haemorrhage between skull and dura mater

Usually due to middle meningeal artery tear

95% have skull fracturefracture

Acute subdural hematoma

Haematoma between dura and brain

Caused by sub-dural bridging vein tear

Poor prognosis

Chronic subdural hematoma

Crescentic low density collection of a chronic

sub-dural haematoma

Note density change from acute SDH

Note pressure effect with Note pressure effect with mid-line shift

Sub arachnoid hemorrhageHyper intense central opacification of basal cisterns.

Classical history ‘thunderclap headache’ and vomiting.

Excluded by LP if not obvious on CT.

Treated by neurosurgical Treated by neurosurgical intravascular coiling of aneurism.

Diffuse neuronal lesions

Examination of CSF (cerebrospinal fluid)

Contraindicated in presence of ICP (intracranial mass lesions)

Serum glucose, calcium, Na+, K+, magnesium

Blood gases and pHBlood gases and pH

Liver and renal functions

Hormones (TSH, T4, cortisol)

Drug levels

Arterial blood gases

HypoglycemiaBlood glucose < 3.5mmol/l (63mg/dl)

Causes; Isophane and Lenti insulins

Chlorpropamide

Non-diabetic spontaneous hypoglycemiaBlood glucose < 3mmol/l (54mg/dl)

Causes; Alcohol, drugs (salicylates, quinine)

Liver and kidney failureLiver and kidney failure

Malaria

Endocrine hypo function

Inborn metabolic errors

Mechanism; impaired gluconeogenesis. Glycogenolysis

Investigations: Serum glucose, C-peptide level, Insulin level

Insulin C peptide (Exogenous insulin)

Insulin C peptide (Insulinoma, sulphonylureas)

Insulin C peptide (drugs, other illnesses)

Hyperglycemia (Non-ketotic)Blood glucose ˃50mmol/l(900mg/dl)

Severe dehydration

Pre-renal uremia

Investigations; Blood glucose, Blood osmolality (measurement)

or by formula

Osmolality; 2[Na+]+2[K+]+[glucose]+[urea]

Blood osmolality in coma ˃340mmol/kg

(Normal value 280-300mmol/kg) (Normal value 280-300mmol/kg)

Hyperglycemia (Ketotic)Smell of acetone, hypothermia, confusion, drowsiness, coma,

air hunger (kussmaul breathing)

Investigations; Blood glucose, urea, electrolytes, HCO3

HCO3<12mmol/l (Normal value 22-32mmol/l)

Arterial blood gases

Urine for ketones

Cerebral malaria (falciparum malaria) comaS/S; Hyperpyrexia

Convulsions

Coma

Marked anemia

Renal failure

Hepatic failure

Hypoglycemia

Acidosis

Pulmonary edema.Pulmonary edema.

Hyperparasitemia>10% RBCs have parasites

Myxoedema comaInvestigations; TSH, T4, Cortisol

CSF; protein

CSF; pressure

Thyroid scan; goiter

Hepatic comaInvestigations; AST, Bilirubin, Prothrombin, Factor V

NH3 levels (inc. sensitivity to dietary proteins)

Glutamic acid 2-oxoglutamate in brain

Short and medium chain fatty acids

Captans in plasma (fetor hepaticus)

Leucine, isoleucine, valine

Uremic comaUremic comaInvestigations; FBG, Smear, Clotting screen

Urea, creatinine, electrolytes

Urine microscopy (dysmorphic RBCs)-casts

Urine protein

Blood cultures

CRP (ESR is misleading in ARF)

Ig & Protein electrophoresis, ACNA, Anti GBM, ANA

(Unknown diagnosis)

Coma in respiratory failureInvestigations; Arterial blood gases paO2 and Pco2

HCO3 level

pH level

Aim; To keep PaO2 > 7kpa (52mmHg) & PCO2 < 5kpa (37mmHg)

Type I; PaO2 < 8kpa (60mmHg)

PCo2 < 6.6kpa (50mmHg)

Causes Acute: Acute severe asthma Chronic: Emphysema

Pulmonary oedema Lung fibrosisPulmonary oedema Lung fibrosis

Brain stem lesions Right to left shunt

Type II; PaO2 < 8kpa (60mmHg)

PCo2 > 6.6kpa (50mmHg)

Causes Acute: Acute severe asthma Chronic: COPD

Acute flare-up COPD Sleep apnea

Acute neuropathies Myopathies

Narcotic drugs

Drug overdose comaQualitative screening of urine; Urine-immunofluorescence

Urine-spot test for drugs

Urine immunofluroescence is used for:

Benzodiazepines

Cocaine

Opioids-Narcotics

Canabis

Amphetamines

Drawbacks; cannot detect fentanyl derivatives, tramadol & synthetic opioids

Spot colour test is used for:

Acetaminophen

Salicylates

Phenothiazines

Imipramine and analogues

Ethchlorovynol

Different separation techniques (TLC, GC, HPLC) are used for screening of a

broad range of drugs. For confirmation of presumptive positive test a quantitative

drug measurement is performed using G-C-MS (Gas chromatography mass

spectroscopy)

Hypoxaemic hypoxia;

low PaO2 in blood due to poor ventilation e.g. CCF

Anaemic hypoxia;

normal PaO2 but low Hb e.g. bleeding

Hypoxic comaHypoxic coma

Primary hypoxia;

failure to deliver O2 e.g. Methaemaglobin or CO poisoning

Ischaemic hypoxia;

cerebral ischaemia / ischaemic heart disease

Management of comatose patient

Maintain adequate cerebral oxygenation; patent

airway, assisted respiration if necessary

Prevent aspiration. Nursing the patient on the side and

empty the stomach

Establish an intravenous line for prompt medication Establish an intravenous line for prompt medication

e.g. IV glucose/insulin, high dose steroid,

anticonvulsants

CASE NO I:

A female patient aged 50 years, was brought to

emergency department in Coma, after 5 hours drive

from a village. Her blood pressure was 145/80

temperature was normal. The attendants gave history

of fever, body aches pains and diarrhea for 7 days

O/E her mouth was deviated slightly to right side. O/E her mouth was deviated slightly to right side.

Her TLC was 1200/ul

Hb 12.4

RBG 35mg/dl

Blood urea 35mg/dl

What further investigation will you carry to reach a final

diagnosis.

CASE NO II:

A 19 years old man was brought to emergency

department in Coma. According to history by the

attendant he presented with a terrible headache the

worse he had even had, nausea and vomiting with

sudden onset. According to him it started after having sudden onset. According to him it started after having

sex with her partner. He takes no medicines, is usually

very fit and well with an un-remarkable PMH.

Comment on your plan of investigations for final

diagnosis.

CASE NO III:

During midnight 69 years old man was brought by his sons to emergency department. He had been unwell, he had a slurred speech. He was neglecting his left side and unable to move his arm and leg. The sons told that his father is a smoker and that he has blood pressure. pressure.

Your plan of investigations to reach the final diagnosis

THANK YOUYOU